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Abstract Children with congenital heart disease (CHD) are living longer due to effective medical and surgical management. However, the majority have neurodevelopmental delays or disorders. The role of the placenta in fetal brain development is unclear and is the focus of an emerging field known as neuroplacentology. In this review, we summarize neurodevelopmental outcomes in CHD and their brain imaging correlates both in utero and postnatally. We review differences in the structure and function of the placenta in pregnancies complicated by fetal CHD and introduce the concept of a placental inefficiency phenotype that occurs in severe forms of fetal CHD, characterized by a myriad of pathologies. We propose that in CHD placental dysfunction contributes to decreased fetal cerebral oxygen delivery resulting in poor brain growth, brain abnormalities, and impaired neurodevelopment. We conclude the review with key areas for future research in neuroplacentology in the fetal CHD population, including (1) differences in structure and function of the CHD placenta, (2) modifiable and nonmodifiable factors that impact the hemodynamic balance between placental and cerebral circulations, (3) interventions to improve placental function and protect brain development in utero, and (4) the role of genetic and epigenetic influences on the placenta–heart–brain connection. Impact Neuroplacentology seeks to understand placental connections to fetal brain development. In fetuses with CHD, brain growth abnormalities begin in utero. Placental microstructure as well as perfusion and function are abnormal in fetal CHD.

Magnetic resonance imaging (MRI) assesses pulmonary hypoplasia in fetal congenital diaphragmatic hernia (CDH). Neonatal mortality may occur with CDH. To quantify MRI parameters associated with neonatal survival in fetuses with isolated CDH. Fetal MRI for assessing CDH included region of interest (ROI) measurements for total lung volume (TLV), herniated liver volume, herniated other organ volume and predicted lung volume. Ratios of observed lung volume and liver up volume to predicted lung volume (observed to predicted TLV, percentage of the thorax occupied by liver) were calculated and compared to neonatal outcomes. Analyses included Wilcoxon rank sum test, multivariate logistic regression and receiver operating characteristic (ROC) curves. Of 61 studies, the median observed to predicted TLV was 0.25 in survivors and 0.16 in non-survivors (P=0.001) with CDH. The median percentage of the thorax occupied by liver was 0.02 in survivors and 0.22 in non-survivors (P 28 weeks was greater compared to GA ≤28 weeks. The ROC analysis demonstrated an area under the curve of 0.96 (95% confidence interval 0.91–1.00) for the combined observed to predicted TLV, percentage of the thorax occupied by liver and GA. The percentage of the thorax occupied by liver and observed to predicted TLV was predictive of neonatal survival in fetuses with CDH.

The objectives of this study were to estimate the rates of sonographically detected anal sphincter defects within 72 h of childbirth and to evaluate intra- and interobserver agreement using three-dimensional (3-D) endoanal sonography data. This is a prospective observational study of primiparous women delivered vaginally. Women without clinically identified anal sphincter lacerations underwent endoanal ultrasonography within 72 h of delivery. Intra- and interobserver agreement for diagnosis of sphincter defects using 3-D endoanal sonography data was calculated using kappa statistics. The rate of sphincter defects in 107 women undergoing 3-D endoanal sonography was 12 %. Characteristics of women with sonographically detected sphincter defects, compared to those without, included a significantly increased rate of clinically diagnosed second-degree lacerations (54 vs 20 %, p 0.008). The intra- and interobserver agreement for diagnosis of sphincter defects using 3-D endoanal sonography data was 0.82 [confidence interval (CI) 0.66–0.99] and 0.72 (CI 0.54–0.92), respectively. Anal sphincter defects detected using endoanal sonography are common, occurring in 12 % of primiparous women, and are significantly associated with other less severe perineal lacerations. Overall and combining sonographically detected defects with clinically diagnosed lacerations, we estimate that 17.8 % of primiparous women delivered vaginally sustain anal sphincter injuries. The intraobserver agreement for diagnosis of sphincter defects is very good and the interobserver agreement is good.

The objective of this study is to describe magnetic resonance (MR) signal intensity (SI) changes in the cervix during pregnancy. This is an observational cohort study of women with a history of preterm delivery. MR imaging sequences were performed every 3 to 4 weeks. Using 8 regions of interest, the SIs are quantified and analyzed with respect to gestational age. Twenty-seven MR studies were performed on a cohort of 8 women. The SIs of the external os are significantly greater than those of the internal os ( P = .035). Similarly, the SIs of the outer stroma are greater than those of the inner stroma (P = .002). As gestational age advances, the inner to outer stromal SI ratio increases, primarily because of a decreasing SI in the outer stromal layer (P = .03). The MR SIs of the cervical stromal zones display variability during pregnancy and decrease with advancing gestation.

Glenoid dysplasia is an anomaly of the scapula characterized by underdevelopment of the bony glenoid and adjacent part of the scapular neck which may be seen as a primary isolated condition, in patients with multiple anomalies or ill-defined syndromes, in well-described syndromes, in mucopolysaccharidoses and related conditions, and in certain skeletal dysplasias. The general subject of glenoid dysplasia is reviewed with reference to descriptions in the literature and personal observations.